PubMed Health⌕ Search

Biomedical subjects

M L Marcos

Publications and source records attributed to M L Marcos.

10 recordsLinked to original sources

Changes in gastrin and serum pepsinogens in monitoring of Helicobacter pylori response to therapy.

The aims of this study in 50 patients with H. pylori infection and duodenal ulcer were to examine the effect of eradication therapy on the serum levels of gastrin, pepsinogen I, and pepsinogen II and to investigate whether monitoring of the serum changes in these peptides after treatment could predict patient outcome. H. pylori status was assessed at entry and one and six months after therapy by culturing and microscopic analysis of the gastric mucosa and by [14C]urea breath test. Significant decreases were observed in the serum levels of gastrin (-11.4 +/- 3%), pepsinogen I (-28.9 +/- 4%), and pepsinogen II (-40.4 +/- 3%) in the 45 patients whose infection was eradicated, but not in the patients without eradication. Serum values of these peptides were unchanged in an additional group of 10 patients that only received omeprazol, none of whom had H. pylori eradicated. The best cutoff point of the percentage of each peptide to predict patient outcome was 10% for gastrin and pepsinogen I, and 15% for pepsinogen II. A pepsinogen II decrease > 15% resulted in the best marker of H. pylori clearance, accurately identifying patient outcome 86.6% of the time, whereas the diagnostic accuracy of gastrin and pepsinogen I was 61.7% and 76.6%, respectively. Significant correlations were found between the bacterial load assessed by histology with the serum concentrations of pepsinogen I and II and with the urease activity as measured by the amount of 14CO2 excreted. In conclusion, eradication of H. pylori infection is followed by a significant drop in serum levels of gastrin, pepsinogen I, and pepsinogen II. Changes in the latter are the most uniform and may be used as an indirect tool to predict treatment outcome.

Adult↗

Effect of sulfonylureas on hepatic glycogen metabolism: activation of glycogen phosphorylase.

In hepatocytes isolated from fed rats, both tolbutamide and glipizide caused a dose-dependent activation of glycogen phosphorylase, possibly by a Ca2+-mediated mechanism. Maximal effects (about twofold) were already obtained when drugs were used at 0.5 mmol/L, the calculated concentrations of tolbutamide and glipizide responsible for the half-maximal effects being 60 and 30 mumol/L, respectively. The activation of glycogen phosphorylase caused the mobilization of glycogen and increased the cellular concentration of hexose 6-phosphates (glucose 6-phosphate plus fructose 6-phosphate) and that of fructose 2,6-bisphosphate. Under the influence of sulfonylureas, glucose formation was slightly stimulated while the rate of L-lactate production was more markedly incremented, indicating that sulfonylureas canalize the metabolic flux coming from glycogen mainly to the glycolytic pathway. These results suggest that a glycogenolytic action of sulfonylureas could collaborate to raise hepatic fructose 2,6-bisphosphate concentration in the fed animal.

Animals↗

Estrogen and progesterone receptors in intracranial tumors.

Cytoplasmic estrogen receptor (ER) and progesterone receptor (PR) proteins were measured by a dextran-coated charcoal absorption technique in 19 intracranial tumors (10 meningiomas, two acoustic neurinomas, two glioblastomas, one primary tumor of neuroectodermal origin, one hemangioblastoma, one metastasis of carcinoma, one chordoma, and one pituitary adenoma). Positive PR values (greater than or equal to 10 fmol/mg of protein) were found in nine meningiomas (90% of these tumors), in the chordoma, in one glioblastoma, and in the hemangioblastoma, whereas positive ER values were recorded only in the pituitary adenoma and in one glioblastoma. Evidence of PR in meningiomas might explain their predominance in women. A possible pharmacological therapy, based on these findings, is discussed.

Adult↗

Estrogen- and progesterone-receptor proteins in intracranial tumors.

Estrogen and progesterone receptors have been measured in 13 intracranial tumors (eight meningiomas, two acoustic neurinomas, one primary tumor of neuroectodermal origin, one giant-celled glioblastoma, and one metastasis of carcinoma). Evidence is provided of the presence of progesterone receptors in meningiomas (87.5%). We could not find clear evidence of estrogen receptors in any tumor of this series. Presence of progesterone receptors in meningiomas suggests an explanation for the greater incidence of these tumors in women and their rapid growth during pregnancy.

Adult↗